ARDC Research Link Australia Research Link Australia   BETA Research
Link
Australia
  • ARDC Newsletter Subscribe
  • Contact Us
  • Home
  • About
  • Feedback
  • Explore Collaborations
  • Researcher
  • Funded Activity
  • Organisation
  • Researcher
  • Funded Activity
  • Organisation
  • Researcher
  • Funded Activity
  • Organisation

Need help searching? View our Search Guide.

Advanced Search

Current Selection
Research Topic : Cell Reprogramming
Scheme : Project Grants
Australian State/Territory : ACT
Status : Closed
Clear All
Filter by Field of Research
Autoimmunity (1)
Biochemistry and Cell Biology not elsewhere classified (1)
Cellular Immunology (1)
Medical Parasitology (1)
Signal Transduction (1)
Filter by Socio-Economic Objective
Search did not return any results.
Filter by Funding Provider
National Health and Medical Research Council (5)
Filter by Status
Closed (5)
Filter by Scheme
Project Grants (5)
Filter by Country
Australia (4)
Filter by Australian State/Territory
ACT (4)
VIC (2)
NSW (1)
WA (1)
  • Researchers (0)
  • Funded Activities (5)
  • Organisations (7)
  • Funded Activity

    Investigating The Cellular Response To Iron-Depletion: The Trilogy Of ASK1, Thioredoxin And Ribonucleotide Reductase

    Funder
    National Health and Medical Research Council
    Funding Amount
    $552,572.00
    Summary
    Iron is crucial for many essential biological processes. Recently, we demonstrated that iron-depletion can affects important signalling pathways (e.g., JNK and p38) that play important roles in growth arrest and apoptosis. This study is designed to investigate the cellular and molecular effects of iron depletion which currently remains unclear. The research is crucial for understanding: (1) the effects of iron deficiency and (2) for understanding the effects of iron chelators that are used for t .... Iron is crucial for many essential biological processes. Recently, we demonstrated that iron-depletion can affects important signalling pathways (e.g., JNK and p38) that play important roles in growth arrest and apoptosis. This study is designed to investigate the cellular and molecular effects of iron depletion which currently remains unclear. The research is crucial for understanding: (1) the effects of iron deficiency and (2) for understanding the effects of iron chelators that are used for treating various diseases.
    Read more Read less
    More information
    Funded Activity

    How Does NF-kB2 Regulate Thymic Selection To Prevent Organ-specific Autoimmune Disease?

    Funder
    National Health and Medical Research Council
    Funding Amount
    $787,600.00
    Summary
    Autoimmune diseases like type 1 diabetes and thyroiditis arise from defects that cause the immune system to confuse self and non-self. Normally, this distinction is programmed in the thymus. We recently identified the gene that causes a form of autoimmune disease. We also made an important discovery about how the thymus gland regulates self-non-self discrimination. We will build on these two discoveries to gain a precise understanding of how the immune system normally avoids autoimmune disease.
    More information
    Funded Activity

    Targeting An Ion Pump In The Malaria Parasite With Multiple Compound Classes

    Funder
    National Health and Medical Research Council
    Funding Amount
    $384,686.00
    Summary
    Large-scale antimalarial drug screening projects have identified three different classes of compound that kill the malaria parasite at extremely low doses and which hold real promise as next-generation antimalarials. Genetic evidence, as well as preliminary data from our own lab, has led us to the hypothesis that all three compound classes exert their antimalarial effect by blocking a molecular ion pump on the parasite surface. The aim of this study is to test this.
    More information
    Funded Activity

    Modeling Human Actin Related Protein 2/3 Complex Subunit 1B (ARPC1B) Deficiency In Mice

    Funder
    National Health and Medical Research Council
    Funding Amount
    $755,005.00
    Summary
    The actin cytoskeleton forms the structure that not only keeps cells in their normal shape but is also essential for the movement of cells and for interaction between cells. We have recently identified the first patients with an immunodeficiency caused by a defect in a gene called ARPC1B, which plays a crucial role in the regulation of actin. Through the investigation of novel mouse models we will elucidate the pathomechanism underlying the disease of these patients.
    More information
    Funded Activity

    MLKL-regulated Necroptosis Pathways In Disease

    Funder
    National Health and Medical Research Council
    Funding Amount
    $610,683.00
    Summary
    Only recently has it emerged that our cells have a built-in backup mechanism that instructs cells to die in extreme cases, such as when viruses have hijacked a cell. A misfiring backup mechanism is thought to underlie a number of human diseases, including inflammatory disease. Our investigation will establish a starting point for the development of novel anti-inflammatory drugs.
    More information

    Showing 1-5 of 5 Funded Activites

    Advanced Search

    Advanced search on the Researcher index.

    Advanced search on the Funded Activity index.

    Advanced search on the Organisation index.

    National Collaborative Research Infrastructure Strategy

    The Australian Research Data Commons is enabled by NCRIS.

    ARDC CONNECT NEWSLETTER

    Subscribe to the ARDC Connect Newsletter to keep up-to-date with the latest digital research news, events, resources, career opportunities and more.

    Subscribe

    Quick Links

    • Home
    • About Research Link Australia
    • Product Roadmap
    • Documentation
    • Disclaimer
    • Contact ARDC

    We acknowledge and celebrate the First Australians on whose traditional lands we live and work, and we pay our respects to Elders past, present and emerging.

    Copyright © ARDC. ACN 633 798 857 Terms and Conditions Privacy Policy Accessibility Statement
    Top
    Quick Feedback